七氟醚显著延长高血糖患者的QTc间期
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Sevoflurane causes greater QTc interval prolongation in chronically hyperglycemic patients than in normoglycemic patients
背景与目的:QTc间期延长是糖尿病患者的一种严重并发症并增加其死亡率。高血糖抑制延迟整流钾通道电流的快速成分（Ikr）而引起心电图QTc间期的延长。同时七氟醚抑制Ikr 引起QTc间期延长。事实上，尖端扭转型室速也发生在七氟醚麻醉期间糖尿病控制不佳的患者身上。
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方法：共纳入了74例患者，包括37例血糖正常的患者（糖化血红蛋白[HbA1c]：<6.5％）（NG组）和37例慢性高血糖患者（HbA1c：≥6.5％）（HG组）。 采用2mg / kg丙泊酚和0.3μg/ kg / min瑞芬太尼进行麻醉诱导，并用2％七氟醚混合40％O2和0.2-0.3μg/ kg / min瑞芬太尼进行麻醉维持。在给予七氟醚之前和之后5,10,30,60,90和120分钟分别测量患者的QT间期和Tp-e间期（T波的峰末间期），并分别按患者的心率来进行校正（QTc间期和Tp-ec间期）。P<0.05被认为具有统计学意义。
结果：在给予七氟醚之前，两组的QTc间期和Tp-ec间期没有明显差异；在给予七氟醚之后，两组的QTc间期随着时间的增加而逐渐延长，且在给药后10分钟明显高于基线值。在给予七氟醚之后90分钟和120分钟HG组的QTc间期明显延长与NG组。两组的Tp-ec间期均未受七氟醚的影响。
结论：我们已经证明七氟醚能显着延长QTc间期，其延长程度慢性高血糖患者与正常血糖患者相比显著增大。虽然Tp-ec间期不受七氟醚的影响，但应注意的是同时阻断钾通道时会增加心律失常的风险。
Kimura S1, Nakao S1, Kitaura A1, Iwamoto T1, Houri K1, Matsushima M1, Hamasaki S1. Sevoflurane causes greater QTc interval prolongation in chronically hyperglycemic patients than in normoglycemic patients. PLoS One. Dec 1，2017 ;12(12):e0188555. doi: 10.1371/journal.pone.0188555. eCollection 2017.
Background:QTc interval prolongation is a serious diabetic complication and increases mortality rate.Hyperglycemia inhibits the rapid component of delayed rectifier potassium channel currents(Ikr) and prolongs the QTc interval on electrocardiograms. Sevoflurane also inhibits the Ikr and causes QTc interval prolongation. In fact, torsade de pointes occurred in a patient with poorly controlled diabetes mellitus during sevoflurane anesthesia.
Methods: We enrolled 74 patients,including 37 normoglycemic patients (glycated hemoglobin [HbA1c]: <6.5%) (NG group) and 37 chronically hyperglycemic patients (HbA1c: 6.5%) (HG group). Anesthesia was induced with 2 mg/kg propofol and 0.3 μg/kg/min remifentanil, and maintained with 2% sevoflurane in 40% O2 and 0.2±0.3 μg/kg/min remifentanil. The QT interval and Tp-e interval (from the peak to the end of the T wave) were measured before and at 5, 10, 30, 60, 90, and 120 min after the administration of sevoflurane and adjusted for the patient's heart rate (QTc and Tp-ec, respectively). P-values of <0.05 were considered statistically significant.
Results:The QTc and the Tp-ec intervals of the two groups did not differ significantly before the administration of sevoflurane. The QTc interval gradually increased with time in both groups and was significantly longer than the baseline value at 10 min after the administration of sevoflurane in both groups. The QTc interval of the HG group was significantly longer than that of the NG group at 90 min and 120 min after the administration of sevoflurane. The Tp-ec interval was not affected by sevoflurane in either group.
Conclusion:We have demonstrated that sevoflurane significantly prolongs the QTc interval, and that the extent of the prolongation is significantly greater in chronically hyperglycemic patients than in normoglycemic patients. Although Tpec is not affected by sevoflurane, it should be noted that the simultaneous blockade of potassium channels would increase the risk of arrhythmias.
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